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Article: Mechanisms and Functional Significance of Stroke-Induced Neurogenesis.

Marlier, Quentin / Verteneuil, Sebastien / Vandenbosch, Renaud / Malgrange, Brigitte

2015 Volume 9, Page(s) 458

Abstract: ... an updated overview of stroke-induced adult neurogenesis, from a cellular and molecular perspective ... Stroke affects one in every six people worldwide, and is the leading cause of adult disability ... neurogenesis and the identification of adult neural stem cells in the late nineties, one promising ...

Abstract	Stroke affects one in every six people worldwide, and is the leading cause of adult disability. After stroke, some limited spontaneous recovery occurs, the mechanisms of which remain largely unknown. Multiple, parallel approaches are being investigated to develop neuroprotective, reparative and regenerative strategies for the treatment of stroke. For years, clinical studies have tried to use exogenous cell therapy as a means of brain repair, with varying success. Since the rediscovery of adult neurogenesis and the identification of adult neural stem cells in the late nineties, one promising field of investigation is focused upon triggering and stimulating this self-repair system to replace the neurons lost following brain injury. For instance, it is has been demonstrated that the adult brain has the capacity to produce large numbers of new neurons in response to stroke. The purpose of this review is to provide an updated overview of stroke-induced adult neurogenesis, from a cellular and molecular perspective, to its impact on brain repair and functional recovery.
Language	English
Publishing date	2015-12-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2015.00458
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Article ; Online: Common and unique mechanisms of Chinese herbal remedies on ischemic stroke mice revealed by transcriptome analyses.

Shen, Yuh-Chiang / Lu, Chung-Kuang / Liou, Kuo-Tong / Hou, Yu-Chang / Lin, Yun-Lan / Wang, Yea-Hwey / Sun, Hsing-Jen / Liao, Ko-Hsun / Wang, Hsei-Wei

Journal of ethnopharmacology

2015 Volume 173, Page(s) 370–382

Abstract: ... the efficacy and molecular mechanisms of action underlying these CHR.: Results: CHR treatment significantly ... unclear.: Materials and methods: Mice were subjected to an acute ischemic stroke to examine ... infarction, and neurological deficits in stroke mice that also paralleled to improvements ...

Abstract	Ethnopharmacological relevance: Four traditional Chinese herbal remedies (CHR) including Buyang Huanwu decoction (BHD), Xuefu Zhuyu decoction (XZD), Tianma Gouteng decoction (TGD) and Shengyu decoction (SYD) are popular used in treating brain-related dysfunction clinically with different syndrome/pattern based on traditional Chinese medicine (TCM) principles, yet their neuroprotective mechanisms are still unclear. Materials and methods: Mice were subjected to an acute ischemic stroke to examine the efficacy and molecular mechanisms of action underlying these CHR. Results: CHR treatment significantly enhanced the survival rate of stroke mice, with BHD being the most effective CHR. All CHR were superior to recombinant tissue-type plasminogen activator (rt-PA) treatment in successfully ameliorating brain function, infarction, and neurological deficits in stroke mice that also paralleled to improvements in blood-brain barrier damage, inflammation, apoptosis, and neurogenesis. Transcriptome analyses reveals that a total of 774 ischemia-induced probe sets were significantly modulated by four CHR, including 52 commonly upregulated genes and 54 commonly downregulated ones. Among them, activation of neurogenesis-associated signaling pathways and down-regulating inflammation and apoptosis pathways are key common mechanisms in ischemic stroke protection by all CHR. Besides, levels of plasma CX3CL1 and S100a9 in patients could be used as biomarkers for therapeutic evaluation before functional recovery could be observed. Conclusion: Our results suggest that using CHR, a combinatory cocktail therapy, is a better way than rt-PA for treating cerebral ischemic-associated diseases through modulating a common as well as a specific group of genes/pathways that may partially explain the syndrome differentiation and treatment principle in TCM.
MeSH term(s)	Animals ; Calgranulin B/genetics ; Chemokine CXCL1/genetics ; Drug Therapy, Combination ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/therapeutic use ; Gene Expression Profiling ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/genetics ; Male ; Medicine, Chinese Traditional ; Mice, Inbred ICR ; Neurogenesis/drug effects ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Phytotherapy
Chemical Substances	Calgranulin B ; Chemokine CXCL1 ; Cxcl1 protein, mouse ; Drugs, Chinese Herbal ; Neuroprotective Agents ; S100A9 protein, mouse ; Xue-Fu-Zhu-Yu decoction ; buyang huanwu ; shengyu ; tianma gouteng
Language	English
Publishing date	2015-09-15
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2015.07.018
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Article: Common and unique mechanisms of Chinese herbal remedies on ischemic stroke mice revealed by transcriptome analyses

Shen, Yuh-Chiang / Chung-Kuang Lu / Hsei-Wei Wang / Hsing-Jen Sun / Ko-Hsun Liao / Kuo-Tong Liou / Yea-Hwey Wang / Yu-Chang Hou / Yun-Lan Lin

Journal of ethnopharmacology. 2015 Sept. 15, v. 173

2015

Abstract: ... apoptosis, and neurogenesis. Transcriptome analyses reveals that a total of 774 ischemia-induced probe sets ... inflammation and apoptosis pathways are key common mechanisms in ischemic stroke protection by all CHR. Besides ... and molecular mechanisms of action underlying these CHR. Results: CHR treatment significantly enhanced ...

Abstract	Ethnopharmacological relevance: Four traditional Chinese herbal remedies (CHR) including Buyang Huanwu decoction (BHD), Xuefu Zhuyu decoction (XZD), Tianma Gouteng decoction (TGD) and Shengyu decoction (SYD) are popular used in treating brain-related dysfunction clinically with different syndrome/pattern based on traditional Chinese medicine (TCM) principles, yet their neuroprotective mechanisms are still unclear. Materials and methods: Mice were subjected to an acute ischemic stroke to examine the efficacy and molecular mechanisms of action underlying these CHR. Results: CHR treatment significantly enhanced the survival rate of stroke mice, with BHD being the most effective CHR. All CHR were superior to recombinant tissue-type plasminogen activator (rt-PA) treatment in successfully ameliorating brain function, infarction, and neurological deficits in stroke mice that also paralleled to improvements in blood–brain barrier damage, inflammation, apoptosis, and neurogenesis. Transcriptome analyses reveals that a total of 774 ischemia-induced probe sets were significantly modulated by four CHR, including 52 commonly upregulated genes and 54 commonly downregulated ones. Among them, activation of neurogenesis-associated signaling pathways and down-regulating inflammation and apoptosis pathways are key common mechanisms in ischemic stroke protection by all CHR. Besides, levels of plasma CX3CL1 and S100a9 in patients could be used as biomarkers for therapeutic evaluation before functional recovery could be observed. Conclusion: Our results suggest that using CHR, a combinatory cocktail therapy, is a better way than rt-PA for treating cerebral ischemic-associated diseases through modulating a common as well as a specific group of genes/pathways that may partially explain the syndrome differentiation and treatment principle in TCM.
Keywords	apoptosis ; biomarkers ; blood-brain barrier ; brain ; chemokine CX3CL1 ; gene expression regulation ; genes ; infarction ; inflammation ; mechanism of action ; mice ; neurogenesis ; Oriental traditional medicine ; patients ; plasminogen activator ; signal transduction ; stroke ; survival rate ; therapeutics
Language	English
Dates of publication	2015-0915
Size	p. 370-382.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2015.07.018
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Article: Unique mechanisms of sheng yu decoction ( shèng yù tang) on ischemic stroke mice revealed by an integrated neurofunctional and transcriptome analysis.

Hou, Yu-Chang / Lu, Chung-Kuang / Wang, Yea-Hwey / Chern, Chang-Ming / Liou, Kuo-Tong / Wang, Hsei-Wei / Shen, Yuh-Chiang

Journal of traditional and complementary medicine

2014 Volume 3, Issue 4, Page(s) 240–249

Abstract: ... and oxidative stress, and significantly improved neurological deficits in mice with stroke. Molecular ... out of 2081 ischemia-induced probe sets were significantly influenced by SYD. Mining the functional ... and mechanisms of action of SYD by an integrated neurofunctional and transcriptome analysis. More ...

Abstract	Sheng Yu Decoction ( Shèng Yù Tang; SYD) is a popular traditional Chinese medicine (TCM) remedy used in treating cardiovascular and brain-related dysfunction clinically; yet, its neuroprotective mechanisms are still unclear. Here, mice were subjected to an acute ischemic stroke to examine the efficacy and mechanisms of action of SYD by an integrated neurofunctional and transcriptome analysis. More than 80% of the mice died within 2 days after ischemic stroke with vehicle treatment. Treatments with SYD (1.0 g/kg, twice daily, orally or p.o.) and recombinant thrombolytic tissue plasminogen activator (rt-PA; 10 mg/kg, once daily, intravenously or i.v.) both significantly extended the lifespan as compared to that of the vehicle-treated stroke group. SYD successfully restored brain function, ameliorated cerebral infarction and oxidative stress, and significantly improved neurological deficits in mice with stroke. Molecular impact of SYD by a genome-wide transcriptome analysis using brains from stroke mice showed a total of 162 out of 2081 ischemia-induced probe sets were significantly influenced by SYD. Mining the functional modules and genetic networks of these 162 genes revealed a significant upregulation of neuroprotective genes in Wnt receptor signaling pathway (3 genes) and regulation of cell communication (7 genes) and downregulation of destructive genes in response to stress (13 genes) and in the induction of inflammation (5 genes), cytokine production (4 genes), angiogenesis (3 genes), vasculature (6 genes) and blood vessel (5 genes) development, wound healing (7 genes), defense response (7 genes), chemotaxis (4 genes), immune response (7 genes), antigen processing and presenting (3 genes), and leukocyte-mediated cytotoxicity (2 genes) by SYD. Our results suggest that SYD could protect mice against ischemic stroke primarily through significantly downregulating the damaging genes involved in stress, inflammation, angiogenesis, blood vessel formation, immune responses, and wound healing, as well as upregulating the genes mediating neurogenesis and cell communication, which make SYD beneficial for treating ischemic stroke.
Language	English
Publishing date	2014-02-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2709698-1
ISSN	2225-4110
ISSN	2225-4110
DOI	10.4103/2225-4110.119703
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Article ; Online: Effects of neural progenitor cells on sensorimotor recovery and endogenous repair mechanisms after photothrombotic stroke.

Minnerup, Jens / Kim, Jeong Beom / Schmidt, Antje / Diederich, Kai / Bauer, Henrike / Schilling, Matthias / Strecker, Jan-Kolja / Ringelstein, E Bernd / Sommer, Clemens / Schöler, Hans R / Schäbitz, Wolf-Rüdiger

Stroke

2011 Volume 42, Issue 6, Page(s) 1757–1763

Abstract: ... functional recovery after experimental stroke. The underlying mechanisms, however, are not completely understood ... so far. Here, we investigated the effects of systemic NPC transplantation on endogenous neurogenesis and ... to 4 weeks after ischemia. Endogenous neurogenesis, dendritic length, and dendritic branching ...

Abstract	Background and purpose: Intravenous neural progenitor cell (NPC) treatment was shown to improve functional recovery after experimental stroke. The underlying mechanisms, however, are not completely understood so far. Here, we investigated the effects of systemic NPC transplantation on endogenous neurogenesis and dendritic plasticity of host neurons. Methods: Twenty-four hours after photothrombotic ischemia, adult rats received either 5 million NPC or placebo intravenously. Behavioral tests were performed weekly up to 4 weeks after ischemia. Endogenous neurogenesis, dendritic length, and dendritic branching of cortical pyramid cells and microglial activation were quantified. Results: NPC treatment led to a significantly improved sensorimotor function measured by the adhesive removal test. The dendritic length and the amount of branch points were significantly increased after NPC transplantation, whereas endogenous neurogenesis was decreased compared to placebo therapy. Decreased endogenous neurogenesis was associated with an increased number of activated microglial cells. Conclusions: Our findings suggest that an increased dendritic plasticity might be the structural basis of NPC-induced functional recovery. The decreased endogenous neurogenesis after NPC treatment seems to be mediated by microglial activation.
MeSH term(s)	Animals ; Behavior, Animal/physiology ; Cell- and Tissue-Based Therapy/methods ; Cells, Cultured ; Mice ; Neural Stem Cells/cytology ; Neural Stem Cells/physiology ; Neural Stem Cells/transplantation ; Neurogenesis/physiology ; Phenotype ; Random Allocation ; Rats ; Recovery of Function/physiology ; Stroke/physiopathology ; Stroke/therapy
Language	English
Publishing date	2011-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80381-9
ISSN	1524-4628 ; 0039-2499 ; 0749-7954
ISSN (online)	1524-4628
ISSN	0039-2499 ; 0749-7954
DOI	10.1161/STROKEAHA.110.599282
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Article ; Online: Deciphering the neuroprotective mechanisms of Bu-yang Huan-wu decoction by an integrative neurofunctional and genomic approach in ischemic stroke mice.

Wang, Hsei-Wei / Liou, Kuo-Tong / Wang, Yea-Hwey / Lu, Chung-Kuang / Lin, Yun-Lian / Lee, I-Jung / Huang, Sheng-Teng / Tsai, Yuan-Hau / Cheng, Yi-Chieh / Lin, Hung-Jui / Shen, Yuh-Chiang

Journal of ethnopharmacology

2011 Volume 138, Issue 1, Page(s) 22–33

Abstract: ... Materials and methods: Male ICR mice were subjected to an acute ischemic stroke by inducing a middle ... and significantly improved the neurological deficits of the mice with a stroke. BHD also reduced ... stroke and extend lifespan primarily through a significant down-regulation of genes involved ...

Abstract	Ethnopharmacological relevance: Bu-yang Huan-wu decoction (BHD) is a famous traditional Chinese medicine formula that has been used clinically in Asia to treat stroke-induced disability for centuries, but the underlying neuroprotective mechanisms are not fully understood. Aim of the study: In this study, we aim to investigate the mechanisms of action using an integrative neurofunctional and broad genomics approach. Materials and methods: Male ICR mice were subjected to an acute ischemic stroke by inducing a middle cerebral ischemic/reperfusion (CI/R) injury. To examine whether BHD could extend the lifespan of mice with a stroke, we used oral administration of BHD (0.5 and 1.0g/kg) twice daily starting from 2h after ischemia and compared this with vehicle control treatments, recombinant tissue-type plasminogen activator (rt-PA, 10mg/kg, i.v.), and MK-801 (0.2mg/kg, i.p.). An integrative neurofunctional and genomic approach was performed to elucidate the underlying molecular mechanisms of BHD. Results: More than 80% of the mice died within 2 days after stroke induction in the vehicle control treatment group. However, the survival rates and life-spans of mice treated with BHD, rt-PA and MK-801 were significantly enhanced as compared to the vehicle-treated CI/R group in all three cases. Mice treated with BHD (1.0g/kg) showed the greatest protective effect across all groups. BHD successfully restored brain function, ameliorated the cerebral infarction, and significantly improved the neurological deficits of the mice with a stroke. BHD also reduced inflammation, oxidative stress, and apoptosis, as well as improved neurogenesis. The molecular impacts of BHD were assessed by genome-wide transcriptome analysis using brains from the CI/R mice. The results showed a total of 377 ischemia-induced probe-sets that were significantly influenced by BHD including 93 probe-sets that were commonly more abundant in BHD-treated and sham mice, and another 284 ischemia-induced probe sets that were suppressed by BHD. Mining the functional modules and genetic networks of these 377 genes revealed a significant upregulation of neuroprotective genes associated with neurogenesis (6 genes) and nervous system development (9 genes), and a significant down-regulation of destructive genes associated with the induction of inflammation (14 genes), apoptosis (15 genes), angiogenesis (11 genes) and blood coagulation (7 genes) by BHD. Conclusions: Our results suggested that BHD is able to protect mice against stroke and extend lifespan primarily through a significant down-regulation of genes involved in inflammation, apoptosis, angiogenesis and blood coagulation, as well as an up-regulation of genes mediating neurogenesis and nervous system development. The changes in expression after treatment with BHD are beneficial after ischemic stroke.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Apoptosis/drug effects ; Apoptosis/genetics ; Astragalus Plant ; Blood Coagulation/drug effects ; Blood Coagulation/genetics ; Brain/drug effects ; Brain/physiology ; Brain Ischemia/drug therapy ; Brain Ischemia/etiology ; Brain Ischemia/genetics ; Cerebral Infarction/prevention & control ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/therapeutic use ; Gene Expression/drug effects ; Inflammation/drug therapy ; Inflammation/genetics ; Male ; Mice ; Mice, Inbred ICR ; Neovascularization, Physiologic/drug effects ; Neovascularization, Physiologic/genetics ; Neurogenesis/drug effects ; Neurogenesis/genetics ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Oxidative Stress/drug effects ; Oxidative Stress/genetics ; Phytotherapy ; Stroke/drug therapy ; Stroke/genetics ; Stroke/mortality ; Tissue Plasminogen Activator/pharmacology
Chemical Substances	Anti-Inflammatory Agents ; Antioxidants ; Drugs, Chinese Herbal ; Neuroprotective Agents ; buyang huanwu ; Tissue Plasminogen Activator (EC 3.4.21.68)
Language	English
Publishing date	2011-10-31
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2011.06.033
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Article: Deciphering the neuroprotective mechanisms of Bu-yang Huan-wu decoction by an integrative neurofunctional and genomic approach in ischemic stroke mice

Wang, Hsei-Wei / Liou, Kuo-Tong / Wang, Yea-Hwey / Lu, Chung-Kuang / Lin, Yun-Lian / Lee, I-Jung / Huang, Sheng-Teng / Tsai, Yuan-Hau / Cheng, Yi-Chieh / Lin, Hung-Jui / Shen, Yuh-Chiang

Journal of ethnopharmacology. 2011 Oct. 31, v. 138, no. 1

2011

Abstract: ... MATERIALS AND METHODS: Male ICR mice were subjected to an acute ischemic stroke by inducing a middle ... and significantly improved the neurological deficits of the mice with a stroke. BHD also reduced ... stroke and extend lifespan primarily through a significant down-regulation of genes involved ...

Abstract	ETHNOPHARMACOLOGICAL RELEVANCE: Bu-yang Huan-wu decoction (BHD) is a famous traditional Chinese medicine formula that has been used clinically in Asia to treat stroke-induced disability for centuries, but the underlying neuroprotective mechanisms are not fully understood. AIM OF THE STUDY: In this study, we aim to investigate the mechanisms of action using an integrative neurofunctional and broad genomics approach. MATERIALS AND METHODS: Male ICR mice were subjected to an acute ischemic stroke by inducing a middle cerebral ischemic/reperfusion (CI/R) injury. To examine whether BHD could extend the lifespan of mice with a stroke, we used oral administration of BHD (0.5 and 1.0g/kg) twice daily starting from 2h after ischemia and compared this with vehicle control treatments, recombinant tissue-type plasminogen activator (rt-PA, 10mg/kg, i.v.), and MK-801 (0.2mg/kg, i.p.). An integrative neurofunctional and genomic approach was performed to elucidate the underlying molecular mechanisms of BHD. RESULTS: More than 80% of the mice died within 2 days after stroke induction in the vehicle control treatment group. However, the survival rates and life-spans of mice treated with BHD, rt-PA and MK-801 were significantly enhanced as compared to the vehicle-treated CI/R group in all three cases. Mice treated with BHD (1.0g/kg) showed the greatest protective effect across all groups. BHD successfully restored brain function, ameliorated the cerebral infarction, and significantly improved the neurological deficits of the mice with a stroke. BHD also reduced inflammation, oxidative stress, and apoptosis, as well as improved neurogenesis. The molecular impacts of BHD were assessed by genome-wide transcriptome analysis using brains from the CI/R mice. The results showed a total of 377 ischemia-induced probe-sets that were significantly influenced by BHD including 93 probe-sets that were commonly more abundant in BHD-treated and sham mice, and another 284 ischemia-induced probe sets that were suppressed by BHD. Mining the functional modules and genetic networks of these 377 genes revealed a significant upregulation of neuroprotective genes associated with neurogenesis (6 genes) and nervous system development (9 genes), and a significant down-regulation of destructive genes associated with the induction of inflammation (14 genes), apoptosis (15 genes), angiogenesis (11 genes) and blood coagulation (7 genes) by BHD. CONCLUSIONS: Our results suggested that BHD is able to protect mice against stroke and extend lifespan primarily through a significant down-regulation of genes involved in inflammation, apoptosis, angiogenesis and blood coagulation, as well as an up-regulation of genes mediating neurogenesis and nervous system development. The changes in expression after treatment with BHD are beneficial after ischemic stroke.
Keywords	angiogenesis ; apoptosis ; blood coagulation ; brain ; gene induction ; genes ; infarction ; inflammation ; longevity ; mechanism of action ; mice ; oral administration ; oxidative stress ; plasminogen activator ; protective effect ; stroke ; survival rate ; traditional medicine ; transcriptome
Language	English
Dates of publication	2011-1031
Size	p. 22-33.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2011.06.033
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Article ; Online: HSPA12B promotes functional recovery after ischaemic stroke through an eNOS-dependent mechanism.

Zhao, Yanlin / Liu, Chang / Liu, Jiali / Kong, Qiuyue / Mao, Yu / Cheng, Hao / Li, Nan / Zhang, Xioajin / Li, Chuanfu / Li, Yuehua / Liu, Li / Ding, Zhengnian

Journal of cellular and molecular medicine

2018 Volume 22, Issue 4, Page(s) 2252–2262

Abstract: ... promoted functional recovery and survival after stroke in an eNOS-dependent mechanism. Targeting HSPA12B ... compared to WT mice. The stroke-induced eNOS phosphorylation and TGF-β1 expression were augmented ... examined 28 days post-stroke) and hippocampal neurogenesis (examined 7 days post-stroke), respectively ...

Abstract	Stroke is the leading cause of disability worldwide. HSPA12B, a heat-shock protein recently identified expression specifically in endothelial cells, is able to promote angiogenesis. Here, we have investigated its effects on functional recovery at chronic phase of ischaemic stroke. Ischaemic stroke was induced by 60 min. of middle cerebral artery occlusion in transgenic mice with overexpression of HSPA12B (HSPA12B Tg) and wild-type littermates (WT). HSPA12B Tg mice demonstrated a significant higher survival rate than WT mice within 28 days post-stroke. Significant improved neurological functions, increased spontaneous locomotor activity and decreased anxiety were detected inHSPA12B Tg mice compared with WT controls within 21 days post-stroke. Stroke-induced hippocampal degeneration was attenuated in HSPA12B Tg mice examined at day 28 post-stroke. Interestingly, HSPA12B Tg mice showed enhanced peri-infarct angiogenesis (examined 28 days post-stroke) and hippocampal neurogenesis (examined 7 days post-stroke), respectively, compared to WT mice. The stroke-induced eNOS phosphorylation and TGF-β1 expression were augmented in HSPA12B Tg mice. However, administration with eNOS inhibitor L-NAME diminished the HSPA12B-induced protection in neurological functional recovery and mice survival post-stroke. The data suggest that HSPA12B promoted functional recovery and survival after stroke in an eNOS-dependent mechanism. Targeting HSPA12B expression may have a therapeutic potential for the stroke-evoked functional disability and mortality.
MeSH term(s)	Animals ; Brain Ischemia/complications ; Brain Ischemia/pathology ; Brain Ischemia/physiopathology ; Cell Proliferation/drug effects ; Enzyme Activation/drug effects ; Enzyme Inhibitors/administration & dosage ; Enzyme Inhibitors/pharmacology ; HSP70 Heat-Shock Proteins/metabolism ; Hippocampus/drug effects ; Hippocampus/pathology ; Hippocampus/physiopathology ; Mice, Transgenic ; NG-Nitroarginine Methyl Ester/pharmacology ; Neovascularization, Physiologic/drug effects ; Neurogenesis/drug effects ; Neurons/drug effects ; Neurons/metabolism ; Nitric Oxide Synthase Type III/antagonists & inhibitors ; Nitric Oxide Synthase Type III/metabolism ; Recovery of Function/drug effects ; Stroke/complications ; Stroke/pathology ; Stroke/physiopathology ; Survival Analysis ; Up-Regulation/drug effects
Chemical Substances	Enzyme Inhibitors ; HSP70 Heat-Shock Proteins ; HSPA12B protein, mouse ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2018-02-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.13507
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Article ; Online: Bone Marrow Endothelial Progenitor Cell Transplantation After Ischemic Stroke: An Investigation Into Its Possible Mechanism.

Bai, Ying-Ying / Peng, Xin-Gui / Wang, Li-Shan / Li, Zi-Hui / Wang, Yuan-Cheng / Lu, Chun-Qiang / Ding, Jie / Li, Pei-Cheng / Zhao, Zhen / Ju, Sheng-Hong

CNS neuroscience & therapeutics

2015 Volume 21, Issue 11, Page(s) 877–886

Abstract: ... along with increased angiogenesis and neurogenesis. On diffusion tensor imaging (DTI), significant ... the observed increases in angiogenesis, neurogenesis, and axonal growth. In addition, the neurons cocultured ... of eNOS and the expression of BDNF were significantly increased in ischemic brain of the EPC-treated mice ...

Abstract	Aims: We tested the hypothesis that endothelial progenitor cell (EPC)-mediated functional recovery after stroke may be associated with the endothelial nitric oxide synthase (eNOS)/brain-derived neurotrophic factor (BDNF) signaling pathway. Methods: Mice were infused with either EPCs or saline after being subjected to middle cerebral artery occlusion. The EPC-treated mice also received intravenous injections of either Nω-nitro-l-arginine methyl ester (L-NAME, the NOS inhibitor) or saline. Results: The activation of eNOS and the expression of BDNF were significantly increased in ischemic brain of the EPC-treated mice, along with increased angiogenesis and neurogenesis. On diffusion tensor imaging (DTI), significant increases in fractional anisotropy and fiber count were observed in white matter, indicating axonal growth stimulated by EPCs. However, the EPC-treated mice that were received an L-NAME injection failed to exhibit the observed increases in angiogenesis, neurogenesis, and axonal growth. In addition, the neurons cocultured with EPCs in vitro exhibited the increased expression of BDNF and decreased apoptosis after oxygen-glucose deprivation compared with the control group. This EPC-induced protective effect was virtually absent in the L-NAME treatment group. Conclusion: The eNOS/BDNF pathway may be involved in the EPC-mediated functional recovery of stroke mice. DTI is feasible for dynamically tracking the orientation of axonal projections after EPC treatment.
MeSH term(s)	Animals ; Bone Marrow Transplantation/methods ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Coculture Techniques ; Disease Models, Animal ; Endothelial Progenitor Cells/physiology ; Endothelial Progenitor Cells/transplantation ; Enzyme Inhibitors/therapeutic use ; Glial Fibrillary Acidic Protein/metabolism ; Infarction, Middle Cerebral Artery/complications ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/surgery ; Male ; Mice ; Mice, Inbred C57BL ; NG-Nitroarginine Methyl Ester/therapeutic use ; Neovascularization, Pathologic/etiology ; Neovascularization, Pathologic/therapy ; Nervous System Diseases/etiology ; Neurogenesis/drug effects ; Neurogenesis/physiology ; Neurons/drug effects ; Nitric Oxide Synthase Type III/metabolism ; Phosphopyruvate Hydratase/metabolism ; Time Factors
Chemical Substances	Brain-Derived Neurotrophic Factor ; Enzyme Inhibitors ; Glial Fibrillary Acidic Protein ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Phosphopyruvate Hydratase (EC 4.2.1.11) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2015-09-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2423467-9
ISSN	1755-5949 ; 1755-5930
ISSN (online)	1755-5949
ISSN	1755-5930
DOI	10.1111/cns.12447
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Ginkgo biloba Extract Prevents Female Mice from Ischemic Brain Damage and the Mechanism Is Independent of the HO1/Wnt Pathway.

Tulsulkar, Jatin / Glueck, Bryan / Hinds, Terry D / Shah, Zahoor A

Translational stroke research

2016 Volume 7, Issue 2, Page(s) 120–131

Abstract: ... to brain damage and loss of functional outcome. We have previously reported neuroprotective properties ... the protective effect of estrogen and were treated with EGb 761 for 7 days prior to inducing permanent ... as compared to the Veh/OVX group and significantly upregulated androgen receptor expression with no changes ...

Abstract	It is well known that gender differences exist in experimental or clinical stroke with respect to brain damage and loss of functional outcome. We have previously reported neuroprotective properties of Ginkgo biloba/EGb 761® (EGb 761) in transient and permanent mouse models of brain ischemia using male mice, and the mechanism of action was attributed to the upregulation of the heme oxygenase 1 (HO1)/Wnt pathway. Here, we sought to investigate whether EGb 761's protective effect in ovariectomized female mice following stroke is also mediated by the HO1/Wnt pathway. Female mice were ovariectomized (OVX) to remove the protective effect of estrogen and were treated with EGb 761 for 7 days prior to inducing permanent middle cerebral artery occlusion (pMCAO) and allowed to survive for an additional 7 days. At day 8, animals were sacrificed, and the brains were harvested for infarct volume analysis, western blots, and immunohistochemistry. The OVX female mice treated with EGb 761 showed significantly lower infarct size as compared to Veh/OVX animals. EGb 761 treatment in female mice inhibited apoptosis by preventing caspase-3 cleavage and blocking the extrinsic apoptotic pathway. EGb 761 pretreatment significantly enhanced neurogenesis in OVX mice as compared to the Veh/OVX group and significantly upregulated androgen receptor expression with no changes in HO1/Wnt signaling. These results suggest that EGb 761 prevented brain damage in OVX female mice by improving grip strength and neurological deficits, and the mechanism of action is not through HO1/Wnt but via blocking the extrinsic apoptotic pathway.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; Brain Infarction/etiology ; Brain Infarction/prevention & control ; Brain Injuries/etiology ; Brain Injuries/physiopathology ; Brain Injuries/prevention & control ; COS Cells ; Caspase 3/metabolism ; Cercopithecus aethiops ; Disease Models, Animal ; Female ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Hand Strength/physiology ; Heme Oxygenase-1/metabolism ; Infarction, Middle Cerebral Artery/complications ; Mice ; Mice, Inbred C57BL ; Neovascularization, Pathologic/etiology ; Neovascularization, Pathologic/prevention & control ; Neurologic Examination ; Ovariectomy ; Plant Extracts/therapeutic use ; Time Factors ; Vascular Endothelial Growth Factor A/metabolism ; Wnt Signaling Pathway/drug effects
Chemical Substances	Plant Extracts ; Vascular Endothelial Growth Factor A ; Ginkgo biloba extract (19FUJ2C58T) ; Heme Oxygenase-1 (EC 1.14.14.18) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2016-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541897-X
ISSN	1868-601X ; 1868-4483
ISSN (online)	1868-601X
ISSN	1868-4483
DOI	10.1007/s12975-015-0433-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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